Effect of Cinnamic Acid on Memory Deficits and Oxidative Stress Induced by Bisphenol A in the Hippocampus of Albino Rats

Bisphenol A (BPA) is known for disrupting the endocrine system. It is used in manufacturing plastic bottles and beverage containers. It binds to hormone receptors and blocks them, leading to various health problems. Cinnamic acid naturally exists in plants and has neuroprotective properties. This investigation assesses cinnamic acid's capacity to enhance memory in BPA-induced neurotoxicity. Forty male rats were grouped as follows: Control as group 1, Group 2 was BPA orally, Group 3 was BPA and cinnamic acid (50 mg/kg), Group 4 was BPA along with cinnamic acid (100 mg/kg), and Group 5 received cinnamic acid alone (100 mg/kg). The treatment spanned 14 days. The behavioral recovery of rats in the groups receiving cinnamic acid and BPA was assessed with the open-field, Y-maze, and grip tests. The study demonstrated that BPA caused oxidative stress in the hippocampus by significantly enhancing lipid peroxidation and decreasing reduced glutathione levels. The antioxidant activities of catalase, glutathione-S- transferase, and superoxide dismutase declined in BPA-treated rats. Nitric oxide levels were significantly high, while acetylcholinesterase activity was non-significantly reduced than the control. Additionally, neurobehavioral deficits were observed in the grip test, with rats spending more time, exhibiting reduced rearing behavior, fewer line crossings, and increased grooming following BPA treatment. Administration of cinnamic acid improved memory by minimizing oxidative stress and inflammation, while enhancing antioxidant activity. This study suggests that cinnamic acid alleviates bisphenol A-induced memory deficits and neuroinflammation through its antioxidant properties.